Clinical Briefs-By Louis Kuritzky, MD
Clinical Briefs-By Louis Kuritzky, MD
NSAIDs and the Risk of Upper Gastrointestinal Bleeding
The use of nonsteroidal anti-inflammatory drugs (NSAIDs) is commonly acknowledged as one of the most important contributors to risk for upper gastrointestinal (GI) bleeding, attributed to inhibition of COX-1. Among the tools used to try to reduce such risk, animal studies have shown that substances that stimulate nitric oxide (NO) in the GI tract may reduce NSAID-induced gastric damage. Since agents like nitroglycerin, a prototypic NO source, are inexpensive, readily available, well tolerated, and thoroughly studied, if similar effects were seen in humans, perhaps GI toxicity of NSAIDs could be reduced. Of concern, however, is the knowledge that NO inhibits platelet aggregation, which in the face of GI bleeding, might retard coagulation and, hence, worsen the problem.
To examine the relationship between NSAIDs and nitrosovasodilators (e.g., nitroglycerin) in respect to GI bleeding, Lanas and colleagues performed a case-control study (n = 3353) comparing persons admitted for GI bleeding with patients admitted for other diagnoses and other local outpatients.
Almost half of persons with GI bleeding had been taking a NSAID in the week before admission. Increased risk of GI bleeding associated with NSAID use ranged from an odds ratio of 7.4 (mostly traditional dose non-COX-1-sparing NSAIDs) to 2.4 (low- dose aspirin), which came as little surprise. On the other hand, use of nitrovasodilators was associated with a statistically significant 0.6 odds ratio of GI bleeding, and even in persons taking a NSAID, nitrovasodilator therapy was associated with a decreased odds ratio of GI bleed. It is hoped that new NO-releasing NSAIDs, which are currently under investigation, will demonstrate favorable effects on GI toxicities.
Lanas A, et al. N Engl J Med 2000; 343:834-839.
Comparative Efficiency of PSA Screening Strategies for Prostate Cancer Detection
Despite the fact that pro- state-specific antigen (PSA) screening has not been proven to reduce mortality from prostate cancer, millions of U.S. men undergo this testing annually in hopes that such screening will have a favorable effect. Sufficient numbers of clinicians have embraced the intuitive positive effect of PSA testing that despite unproven efficacy, using PSA screening has become perceived more as the norm than the exception. In an effort to evaluate, by means of a statistical marker, which modifications of PSA screening might enhance its efficacy, Ross and colleagues compared several PSA screening strategies in this trial.
Considerations focused upon the PSA threshold for prostate biopsy (i.e., the PSA level at which biopsy would be recommended), the frequency of PSA testing (testing interval), and age of PSA testing initiation.
According to Ross et al’s statistical model, if PSA testing were to begin at age 40-45 (instead of the more traditional 50 years of age), followed by testing every two years at age 50, mortality would be favorably affected, with fewer PSA tests and biopsies. On the other hand, if the threshold for biopsy of the prostate were to be reduced below a PSA level of 4.0 ng/mL, no measurable net benefit would be anticipated.
Ross KS, et al. JAMA 2000;284:1399-1405.
White Coat Effect of Alcohol
The lifestyle habit of imbibing alcohol in moderation has been associated with a reduced risk of ischemic heart disease, attributed to such benefits as an improved HDL cholesterol. On the other hand, the relationship between alcohol consumption and elevated blood pressure has also been consistently noted. Since one reason that the alcohol-blood pressure relationship has not led to anticipated negative heart disease impact might be that alcohol induces spurious, or transient, BP elevations, Ryan and Howes studied the relationship between alcohol intake and clinic, as well as ambulatory monitored blood pressure.
The study group included 121 adult men with either controlled hypertension (77%) or who were normotensive. Persons with established liver disease were excluded. More than half of participants consumed alcohol daily. Alcohol consumption was not related to the systolic blood pressure as measured by ambulatory monitoring, but was associated with clinic systolic blood pressure. Ryan and Howes suggest that much of the relationship between alcohol consumption and blood pressure is attributable to the white coat effect, as ambulatory pressure is not related. Additionally, for persons in whom clinic and ambulatory blood pressure show marked discrepancy, a case can be made for investigation of alcohol intake as an explanation.
Ryan WM, Howes LG. Am J Hypertens 2000;13:1135-1138.
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